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Titolo:
Cerebral T-1 rho relaxation time increases immediately upon global ischemia in the rat independently of blood glucose and anoxic depolarization
Autore:
Kettunen, MI; Grohn, OHJ; Penttonen, M; Kauppinen, RA;
Indirizzi:
Univ Kuopio, AI Virtanen Inst Mol Sci, Cognit Neurobiol Lab, Natl Bio NMR Facil, FIN-70211 Kuopio, Finland Univ Kuopio Kuopio Finland FIN-70211 MR Facil, FIN-70211 Kuopio, Finland
Titolo Testata:
MAGNETIC RESONANCE IN MEDICINE
fascicolo: 3, volume: 46, anno: 2001,
pagine: 565 - 572
SICI:
0740-3194(200109)46:3<565:CTRRTI>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
MAGNETIC-RESONANCE SPECTROSCOPY; APPARENT DIFFUSION-COEFFICIENT; WATER DIFFUSION; HYPERCAPNIC RATS; LACTATE CONTENT; ENERGY FAILURE; ROTATING-FRAME; BRAIN ISCHEMIA; T-1; STATE;
Keywords:
brain; ischemia; glucose; MRI; T-1 rho; diffusion;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Kauppinen, RA Univ Kuopio, AI Virtanen Inst Mol Sci, Cognit Neurobiol Lab,Natl Bio NMR Facil, POB 1627, FIN-70211 Kuopio, Finland Univ Kuopio POB 1627 Kuopio Finland FIN-70211 opio, Finland
Citazione:
M.I. Kettunen et al., "Cerebral T-1 rho relaxation time increases immediately upon global ischemia in the rat independently of blood glucose and anoxic depolarization", MAGN RES M, 46(3), 2001, pp. 565-572

Abstract

Time-dependent changes of T-1 in the rotating frame (T-1 rho), diffusion, T-2, and magnetization transfer contrast on cardiac arrest-induced global ischemia in rat were investigated. T-1 rho, a acquired with spin lock amplitudes >0.6 G, started to increase 10-20 sec after cardiac arrest followed byan increase within 3-4 min to a level that was 6-8% greater than in normalbrain. The ischemic T-1 rho response coincided with the drop of water diffusion coefficient in normoglycemic animals. However, unlike the rate of diffusion, the kinetics of T-1 rho were not affected by either preischemic hypoglycemia or hyperglycemia. Similar to diffusion, the kinetics of anoxic depolarization were dependent on preischemic blood glucose levels. Ischemia caused a reduction in the Hahn spin echo T-2 as a result of blood oxygenation level-dependent (BOLD) effect; maximal negative BOLD seen by 40 sec. In the animals injected with an ironoxide particle contrast agent, AMI-227, prior to the insult, both T-1 rho and T-2 immediately increased in concert on induction of ischemia. In contrast to the T-1 rho and diffusion changes, a much slower change in magnetization transfer contrast was evident over the first 20 min of ischemia. These data demonstrate that T-1 rho immediately increases following ischemia and that the pathophysiological mechanisms affecting this relaxation time may not directly involve magnetization transfer. The mechanisms prolonging T-1 rho differ from those affecting water diffusion with respect to their sensitivities to glucose and are apparently independent of membrane depolarization. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/11/20 alle ore 11:46:37